Fetal Programming of Vascular Disease
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The normal fetal development and growth is greatly dependent on the fetal, maternal and placental health. The organs and tissues of a developing fetus go through a stage called 'critical' periods of development. During this critical period, the fetus' cells are dividing very rapidly. "Programming" occurs at this critical period if a stimulus has an everlasting or lifelong effect (Barker, 1998). 'Fetal Origins of Adult Disease' or 'Barker hypothesis' indicates that exposure of a fetus to adverse environment, stimulus or insult in critical periods leads to permanent physiological changes (programming) with loss of plasticity and a fixed functional capacity of tissues within the fetus (Barker, 1998). Fetuses that experience an adverse event during their development may be born small for their gestational age (SGA). In various studies it has been shown that there is a link between low birth weight and disease in adult life. Intrauterine Growth Restriction (IUGR) is the condition in which the fetal growth rate is in the low 10th percentile. IUGR is a disease responsible for neonatal morbidity and mortality and perinatal death affecting 8-10% of all pregnancies. IUGR is an important risk factor for development of cardiovascular disease, type 2 diabetes (Barker, 1998), respiratory distress syndrome, intraventricular hemorrhage and death (Bernstein IM, 2000). In pregnancies complicated by IUGR there is severe placental vascular insufficiency which causes hypoxic environment in the placenta and umbilical cord (Ana Sofia Cerdeira, 2012). The hypoxia causes structural changes in the smooth muscle cells in the medial of the blood vessel wall. In our study, we looked at various structural and morphological changes in the umbilical vessels of the IUGR fetuses by looking at their cell density and measured proliferation of smooth muscles. We measured the medical thickness of the umbilical vessels. We measured the intensity of Endothelial Nitric Oxide Synthase (eNOS) expression in the apical, basal and lateral sections of the placenta as well as the umbilical vessels. We measured the intensity and expression of these early markers such as elastin, collagen and eNOS in placenta and umbilical vessels.